Haematological changes in patients with the new coronavirus pneumonia

SARS-CoV-2 (or 2019-nCoV) has mainly surfaced in the form of respiratory diseases, such as pneumonia. However, there is a range of clinical manifestations observed among infected patients, haematological changes being one of them. Here we give you findings that point out haematology-related changes in infected patients and the associated risks they face.

The Neo Coronavirus pneumonia is the most common form of illness seen among the infected. However, given its global outbreak, clinicians and researchers are discovering a range of other manifestations of the virus in patients with COVID-19. While the nature of the diseases manifesting may be different, an assumption that there may have been pre-existing conditions or higher susceptibility due to age (and therefore, lower immunity) has to be kept in mind.

Given below are the haematological changes observed in patients with COVID-19 pneumonia.

Criterion of diagnosis

According to the seventh edition of the New Coronavirus Pneumonia Diagnosis and Treatment Program, the lymphocyte count has been revised to diagnose the changes in blood samples of patients with NCOVID pneumonia.

The lymphocyte count has been changed to ‘normal or decreased’, which would indicate severe peripheral haemolymph, a progressive reduction in cells and an elevation in D-dimer. Reports of autopsy and biopsy of these patients also revealed a reduction in the number of lymphocytes in the spleen and lymph nodes, lower CD4+ and CD8+T cells, and a decrease in the number of bone marrow tertiary cells. [1]

Risks among patients of the new coronavirus pneumonia

Normally patients of COVID-19 pneumonia may show either of the following symptoms: fever, cough, fatigue, and dyspnoea. However, multiple reports suggest that patients who were critically ill and displayed severe virus-related symptoms were also diagnosed with coagulation dysfunction in varying severities. [2] The risks these patients face in reference to haematology are as under:

Risk of thrombosis

While thrombosis in COVID-19 patients has still not been reported, that the patients run the risk cannot be ruled out. The risk is higher among COVID-19 patients, who have severe symptoms. Approximately 50% of the infected patients display elevated D-dimer levels while the disease progresses. However, the proportion of this incidence was noticed to be as high as 100% in cases of patients who died.

D-dimer levels were found to be higher in patients with severe COVID-19 symptoms in comparison to those who showed milder symptoms. But, the condition of some patients worsened during treatment and they died. This suggests that the risk of thrombosis runs high in patients with severe symptoms.

Risk of diffuse microvascular damage

Multiple organ failure triggered due to diffuse microvascular damage has been identified as one of the major causes of deaths in COVID-19 patients, whose condition was critical. An analysis of 21 patients, who died due to coronavirus, states that 71.4% of them had died with dominant disseminated intravascular coagulation (DIC). The median time from admission to the discovery of combined DIC was 4 days. The incidence of DIC in patients still alive was a mere 0.6%.

Reports also suggest that coagulation disorders and DIC problems in patients with severe COVID-19 are prominent and hence, it can be concluded that the two are important causes of death in patients with coronavirus.

Risk of increased bleeding

It has been observed that incidences of thrombocytopenia in dead patients were as high as 57.1%. Furthermore, factors such as the consumption of platelets and coagulation increase the risk of bleeding in infected patients.

Although COVID-19 patients are said to be prone to coagulation dysfunction, there is still no data available on the number of patients who reported bleeding and thrombosis. [3, 4] There is, however, some literature available that reports abnormal coagulation indicators in the form of fibrinogen degradation products (FDP) and D-dimer levels.

The degree of dimer elevation was noted to be higher in severe patients. So it is highly likely that fibrinogen count could rise during the course of treatment in patients with mild symptoms and those showing early onset of severe infection. The same could lower to a great extent in the late stages for patients with severe infection symptoms.

It was reported that 30% of the patients had shortened prothrombin time (PT) and 16% had shortened activated partial thromboplastin time (APTT). The number of patients with prolonged PT was a mere 5% and that with APTT was 6%. Most COVID-19 patients display a normal to slightly elevated platelet count, but their mean levels cannot be determined in cases of patients with severe infection symptoms and those with milder symptoms.

Factors that play a role

The reason behind coagulopathy in COVID-19 patients could be associated with the infection, inflammatory factor storm, hematopoietic system damage, ischaemia and hypoxia-reperfusion injury, drugs, and other operational factors. The prime pathogenic mechanism of coagulation could be linked to the inflammatory factor storm caused by an immune imbalance in the infected patients after the outbreak of COVID-19. But more pathological research and in-depth study needs to be done to determine the exact cause.

Preventive measures

Patients who are critically ill can die if they start showing an abnormal coagulation function. So early dynamic monitoring to enable timely diagnosis and taking preventive measures become very important.

Critically ill patients should be closely monitored to identify any seemingly fatal clinical indicators. Timely diagnosis can also help protect them from the mal-effects of coagulation dysfunction and death, even.

This story is part of our Global Content Initiative, where we feature selected stories from our Global network which we believe would be most useful and informative to our doctor members. This version is a literal translation of the Chinese version. To access the original article click here.

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